This research seeks to discover the mechanism responsible for cerebral vasospasm following subarachnoid hemorrhage in patients with ruptured intracranial aneurysms. On the basis of past work of the investigators and others, the platelet fraction of blood has been identified as the source of cerebral vasospasm. Our studies have attempted to identify the platelet agent or agents that lead to this disorder. We believe that serotonin (and prostaglandians), may be those agents. Using in vivo and in vitro studies we are attempting to confirm or deny the role of serotonin as the primary cause. Our corollary study is a clinical evaluation of pharmacologic prevention of vasospasm in patients. This is based on our observation that reserpine and kanamycin will completely inhibit the development of vasospasm in experimental animals, whatever the mechanism may be. Ancillary studies have been carried out to determine the role of serotonin and other brain monoamines in the development of vasospasm and cerebral infraction, as a result of injury or stroke.